Amaurosis fugax
BASIC INFORMATION
Amaurosis fugax ("fleeting blindness") is usually caused by retinal emboli from ipsilateral carotid disease. The visual loss is usually described as a curtain passing vertically across the visual field with complete monocular visual loss lasting a few minutes and a similar curtain effect as the episode passes. To reduce the risk of stroke, patients with high-grade stenosis (70-99%) of the ipsilateral internal carotid artery should be considered for carotid endarterectomy or angioplasty with stenting. Patients with medium-grade (30-69%) stenosis, unless there are other risk factors for stroke, or low-grade (up to 29%) stenosis are generally better treated medically with aspirin or other antiplatelet drugs. The most reliable method of evaluating carotid stenosis is intra-arterial angiography, but this is associated with a number of complications including stroke. The noninvasive techniques of duplex ultrasonography and magnetic resonance angiography are suitable screening methods. Emboli from cardiac sources may also be responsible for amaurosis fugax. Electrocardiography should be performed in all cases, particularly to identify atrial fibrillation. Echocardiography should be undertaken in young patients and in any patient with clinical evidence of a potential cardiac source of emboli. In younger patients without carotid or cardiac disease, amaurosis fugax may be due to choroidal or retinal vascular spasm, in which case calcium channel blockers such as slow-release nifedipine, 60 mg/d, appear to be effective. Antiphospholipid syndrome should be excluded.
Amaurosis fugax ("fleeting blindness") is usually caused by retinal emboli from ipsilateral carotid disease. The visual loss is usually described as a curtain passing vertically across the visual field with complete monocular visual loss lasting a few minutes and a similar curtain effect as the episode passes. To reduce the risk of stroke, patients with high-grade stenosis (70-99%) of the ipsilateral internal carotid artery should be considered for carotid endarterectomy or angioplasty with stenting. Patients with medium-grade (30-69%) stenosis, unless there are other risk factors for stroke, or low-grade (up to 29%) stenosis are generally better treated medically with aspirin or other antiplatelet drugs. The most reliable method of evaluating carotid stenosis is intra-arterial angiography, but this is associated with a number of complications including stroke. The noninvasive techniques of duplex ultrasonography and magnetic resonance angiography are suitable screening methods. Emboli from cardiac sources may also be responsible for amaurosis fugax. Electrocardiography should be performed in all cases, particularly to identify atrial fibrillation. Echocardiography should be undertaken in young patients and in any patient with clinical evidence of a potential cardiac source of emboli. In younger patients without carotid or cardiac disease, amaurosis fugax may be due to choroidal or retinal vascular spasm, in which case calcium channel blockers such as slow-release nifedipine, 60 mg/d, appear to be effective. Antiphospholipid syndrome should be excluded.
• Systemic disorders: migraine, giant cell arteritis, blood dyscrasia
WORKUP
• Careful examination of retina; embolus may be visible and confirm the diagnosis
• Auscultation of arteries for bruits
• Examination of all pulses
LABORATORY TESTS
• CBC with sedimentation rate.
• PT and PTT.
• Serum chemistries, including lipid profile.
• Anticardiolipin antibody, protein C, and protein S should be considered in younger patients with a personal or family history of coagulopathy or strokes at a young age.
• VDRL and toxicology screen are discretionary tests based on patient’s age and history.
WORKUP
• Careful examination of retina; embolus may be visible and confirm the diagnosis
• Auscultation of arteries for bruits
• Examination of all pulses
LABORATORY TESTS
• CBC with sedimentation rate.
• PT and PTT.
• Serum chemistries, including lipid profile.
• Anticardiolipin antibody, protein C, and protein S should be considered in younger patients with a personal or family history of coagulopathy or strokes at a young age.
• VDRL and toxicology screen are discretionary tests based on patient’s age and history.
IMAGING STUDIES
• Carotid Dopplers followed by MRA or four-vessel angiography as indicated.
• Transthoracic echocardiography (TTE) is indicated to screen for embolization in patients with evidence of heart disease and in patients without an evident source for their transient neurologic deficit. Transesophageal echocardiography (TEE) is more sensitive for detecting cardiac sources of embolization (ventricular mural thrombus, patent foramen ovale, aortic arch, mitral valve disorders); however, it is more uncomfortable and expensive and is best reserved for patients with an unknown source of TIA or when cardiac embolization cannot be completely ruled out on TTE.
TREATMENT
NONPHARMACOLOGIC THERAPY
• Diet (decrease saturated fatty acids and high-cholesterol foods)
• Exercise
• Cessation of tobacco use if thought to be atherosclerotic in origin
ACUTE GENERAL Rx
• Treat as an emergency.
• Give aspirin, heparin if there is no intracranial hemorrhage.
CHRONIC Rx
Reduce risks by carotid endarterectomy if stenosis >80%. Control hypertension and manage risk factors for increased cholesterol levels.
DISPOSITION
If significant stenosis not found and emboli are from carotid, consider other causes in differential diagnosis.
REFERRAL
Vascular surgeon or neurosurgeon if significant stenosis found
• Carotid endarterectomy is indicated in the following settings:
1. High-grade (=80%) isolateral stenosis and surgery can be done early and at low risk
2. Greater than 50% stenosis associated with a large carotid artery ulcer
3. Multiple TIAs despite medical therapy, in the setting of high-grade or ulcerative ipsilateral disease, and surgery can be done at low to medium risk
4. Crescendo attacks in the setting of high-grade or ulcerative ipsilateral disease and surgery can be done at low to medium risk
• Patient preference and the experience of the surgical team should be considered whenever surgery is contemplated.
• Carotid Dopplers followed by MRA or four-vessel angiography as indicated.
• Transthoracic echocardiography (TTE) is indicated to screen for embolization in patients with evidence of heart disease and in patients without an evident source for their transient neurologic deficit. Transesophageal echocardiography (TEE) is more sensitive for detecting cardiac sources of embolization (ventricular mural thrombus, patent foramen ovale, aortic arch, mitral valve disorders); however, it is more uncomfortable and expensive and is best reserved for patients with an unknown source of TIA or when cardiac embolization cannot be completely ruled out on TTE.
TREATMENT
NONPHARMACOLOGIC THERAPY
• Diet (decrease saturated fatty acids and high-cholesterol foods)
• Exercise
• Cessation of tobacco use if thought to be atherosclerotic in origin
ACUTE GENERAL Rx
• Treat as an emergency.
• Give aspirin, heparin if there is no intracranial hemorrhage.
CHRONIC Rx
Reduce risks by carotid endarterectomy if stenosis >80%. Control hypertension and manage risk factors for increased cholesterol levels.
DISPOSITION
If significant stenosis not found and emboli are from carotid, consider other causes in differential diagnosis.
REFERRAL
Vascular surgeon or neurosurgeon if significant stenosis found
• Carotid endarterectomy is indicated in the following settings:
1. High-grade (=80%) isolateral stenosis and surgery can be done early and at low risk
2. Greater than 50% stenosis associated with a large carotid artery ulcer
3. Multiple TIAs despite medical therapy, in the setting of high-grade or ulcerative ipsilateral disease, and surgery can be done at low to medium risk
4. Crescendo attacks in the setting of high-grade or ulcerative ipsilateral disease and surgery can be done at low to medium risk
• Patient preference and the experience of the surgical team should be considered whenever surgery is contemplated.
Similar episodes of loss of vision, characteristically on exposure to bright light, may occur with poor ocular perfusion usually due to severe occlusive carotid disease. More transient episodes (lasting only a few seconds to 1 minute) affecting both eyes occur in patients with raised intracranial pressure. In all cases of episodic visual loss, early ophthalmologic consultation is advisable.
EPIDEMIOLOGY & DEMOGRAPHICS
INCIDENCE (IN U.S.): An uncommon presentation of carotid artery disease
PEAK INCIDENCE: 55 yr and older
PHYSICAL FINDINGS & CLINICAL PRESENTATION
• There are usually no physical findings.
• Acute stage: cholesterol emboli may be seen in retinal artery (Hollenhorst plaque): carotid bruits or other evidence of generalized atherosclerosis.
• If embolus is cardiac in origin, atrial fibrillation is often present.
ETIOLOGY
Usually embolic
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
• Embolic from carotid artery, aorta and great vessels, heart
• Ocular causes: glaucoma, central retinal vein or artery occlusion
• Neurologic causes: optic neuritis, multiple sclerosis, optic nerve compression
EPIDEMIOLOGY & DEMOGRAPHICS
INCIDENCE (IN U.S.): An uncommon presentation of carotid artery disease
PEAK INCIDENCE: 55 yr and older
PHYSICAL FINDINGS & CLINICAL PRESENTATION
• There are usually no physical findings.
• Acute stage: cholesterol emboli may be seen in retinal artery (Hollenhorst plaque): carotid bruits or other evidence of generalized atherosclerosis.
• If embolus is cardiac in origin, atrial fibrillation is often present.
ETIOLOGY
Usually embolic
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
• Embolic from carotid artery, aorta and great vessels, heart
• Ocular causes: glaucoma, central retinal vein or artery occlusion
• Neurologic causes: optic neuritis, multiple sclerosis, optic nerve compression
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